FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2017005530> ?p ?o ?g. }

• W2017005530 endingPage "156" @default.
• W2017005530 startingPage "146" @default.
• W2017005530 abstract "The accumulation of hydrophobic bile acid, such as glycochenodeoxycholic acid (GCDCA), in the liver has been thought to induce hepatocellular damage in human chronic cholestatic liver diseases. We previously reported that GCDCA-induced apoptosis was promoted by both mitochondria-mediated and endoplasmic reticulum (ER) stress-associated pathways in rat hepatocytes. In this study, we elucidated the relationship between these pathways in GCDCA-induced apoptotic HepG2 cells. HepG2 cells were treated with GCDCA (100-500microM) with or without a caspase-8 inhibitor, Z-IETD-fluoromethyl ketone (Z-IETD-FMK) (30microM) for 3-24h. We demonstrated the presence of both apoptotic pathways in these cells; that is, we showed increases in cleaved caspase-3 proteins, the release of cytochrome c from mitochondria, and the expression of ER resident molecular chaperone Bip mRNA and ER stress response-associated transcription factor Chop mRNA. On the other hand, pretreatment with Z-IETD-FMK significantly reduced the increases, compared with treatment with GCDCA alone. Immunofluorescence microscopic analysis showed that treatment with GCDCA increased the cleavage of BAP31, an integral membrane protein of ER, and pretreatment with Z-IETD-FMK suppressed the increase of caspase-8 and BAP31 cleavage. In conclusion, these results suggest that intact activated caspase-8 may promote and amplify the ER stress response by cleaving BAP31 in GCDCA-induced apoptotic cells." @default.
• W2017005530 created "2016-06-24" @default.
• W2017005530 creator A5009850116 @default.
• W2017005530 creator A5044960251 @default.
• W2017005530 creator A5056826221 @default.
• W2017005530 creator A5058614084 @default.
• W2017005530 creator A5091149562 @default.
• W2017005530 date "2007-11-01" @default.
• W2017005530 modified "2023-10-05" @default.
• W2017005530 title "Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells" @default.
• W2017005530 cites W1506642042 @default.
• W2017005530 cites W1554427046 @default.
• W2017005530 cites W1566777539 @default.
• W2017005530 cites W1964272444 @default.
• W2017005530 cites W1965727325 @default.
• W2017005530 cites W1973007354 @default.
• W2017005530 cites W1974572767 @default.
• W2017005530 cites W1982421412 @default.
• W2017005530 cites W1984547206 @default.
• W2017005530 cites W1988047953 @default.
• W2017005530 cites W1994611236 @default.
• W2017005530 cites W2010334438 @default.
• W2017005530 cites W2011058633 @default.
• W2017005530 cites W2019369579 @default.
• W2017005530 cites W2031499528 @default.
• W2017005530 cites W2032417513 @default.
• W2017005530 cites W2037665471 @default.
• W2017005530 cites W2044020591 @default.
• W2017005530 cites W2054260525 @default.
• W2017005530 cites W2054438783 @default.
• W2017005530 cites W2059912335 @default.
• W2017005530 cites W2061736304 @default.
• W2017005530 cites W2074108834 @default.
• W2017005530 cites W2077068871 @default.
• W2017005530 cites W2078824404 @default.
• W2017005530 cites W2092468599 @default.
• W2017005530 cites W2096220505 @default.
• W2017005530 cites W2110797810 @default.
• W2017005530 cites W2129713991 @default.
• W2017005530 cites W2136269288 @default.
• W2017005530 cites W2155884826 @default.
• W2017005530 cites W2168413006 @default.
• W2017005530 doi "https://doi.org/10.1016/j.tox.2007.08.095" @default.
• W2017005530 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17928124" @default.
• W2017005530 hasPublicationYear "2007" @default.
• W2017005530 type Work @default.
• W2017005530 sameAs 2017005530 @default.
• W2017005530 citedByCount "37" @default.
• W2017005530 countsByYear W20170055302012 @default.
• W2017005530 countsByYear W20170055302014 @default.
• W2017005530 countsByYear W20170055302015 @default.
• W2017005530 countsByYear W20170055302016 @default.
• W2017005530 countsByYear W20170055302017 @default.
• W2017005530 countsByYear W20170055302018 @default.
• W2017005530 countsByYear W20170055302019 @default.
• W2017005530 countsByYear W20170055302020 @default.
• W2017005530 countsByYear W20170055302021 @default.
• W2017005530 countsByYear W20170055302022 @default.
• W2017005530 countsByYear W20170055302023 @default.
• W2017005530 crossrefType "journal-article" @default.
• W2017005530 hasAuthorship W2017005530A5009850116 @default.
• W2017005530 hasAuthorship W2017005530A5044960251 @default.
• W2017005530 hasAuthorship W2017005530A5056826221 @default.
• W2017005530 hasAuthorship W2017005530A5058614084 @default.
• W2017005530 hasAuthorship W2017005530A5091149562 @default.
• W2017005530 hasConcept C139447449 @default.
• W2017005530 hasConcept C153911025 @default.
• W2017005530 hasConcept C158617107 @default.
• W2017005530 hasConcept C185592680 @default.
• W2017005530 hasConcept C190283241 @default.
• W2017005530 hasConcept C29311851 @default.
• W2017005530 hasConcept C31573885 @default.
• W2017005530 hasConcept C48297814 @default.
• W2017005530 hasConcept C55493867 @default.
• W2017005530 hasConcept C86803240 @default.
• W2017005530 hasConcept C95444343 @default.
• W2017005530 hasConcept C98424977 @default.
• W2017005530 hasConceptScore W2017005530C139447449 @default.
• W2017005530 hasConceptScore W2017005530C153911025 @default.
• W2017005530 hasConceptScore W2017005530C158617107 @default.
• W2017005530 hasConceptScore W2017005530C185592680 @default.
• W2017005530 hasConceptScore W2017005530C190283241 @default.
• W2017005530 hasConceptScore W2017005530C29311851 @default.
• W2017005530 hasConceptScore W2017005530C31573885 @default.
• W2017005530 hasConceptScore W2017005530C48297814 @default.
• W2017005530 hasConceptScore W2017005530C55493867 @default.
• W2017005530 hasConceptScore W2017005530C86803240 @default.
• W2017005530 hasConceptScore W2017005530C95444343 @default.
• W2017005530 hasConceptScore W2017005530C98424977 @default.
• W2017005530 hasIssue "3" @default.
• W2017005530 hasLocation W20170055301 @default.
• W2017005530 hasLocation W20170055302 @default.
• W2017005530 hasOpenAccess W2017005530 @default.
• W2017005530 hasPrimaryLocation W20170055301 @default.
• W2017005530 hasRelatedWork W1032990304 @default.
• W2017005530 hasRelatedWork W1980517164 @default.
• W2017005530 hasRelatedWork W1994682335 @default.
• W2017005530 hasRelatedWork W1995301389 @default.

• next